crossing96/oncoscreening huggingface dataset:
Usefulness of CA 125 as a preoperative prognostic marker for transitional cell carcinoma of the bladder.	PURPOSE: We evaluated the role of CA 125 as a prognostic marker in patients with transitional cell carcinoma (TCC) of the bladder undergoing uniform radical cystectomy with bilateral pelvic iliac lymphadenectomy. MATERIALS AND METHODS: From April 1996 to March 2001, 287 patients with a median age of 68 years (range 34 to 89) had preoperative CA 125 serum assays performed. All patients had high grade or invasive TCC and were scheduled to undergo radical cystectomy. Preoperative CA 125 was evaluated according to tumor grade and pathological subgroups (organ confined, extravesical and lymph node positive) as well as recurrence-free and overall survival. RESULTS: Of the 287 patients 31 (10.8%) demonstrated increased serum CA 125 (greater than 35 U/ml). No significant association was found between increased CA 125 and recurrence-free survival or tumor grade. However, a statistically significant association was found among pathological tumor subgroups, namely 4.9% for organ confined, 11.3% for extravesical and 21.6% for lymph node positive disease (p <0.001). Furthermore, patients with lymph node positive disease or high grade tumors (grades III/IV and IV/IV) and increased CA 125 assays demonstrated significantly worse overall survival (p <0.001). CONCLUSIONS: Increased CA 125 was seen in approximately 11% of patients with high grade or invasive TCC preoperatively. It was more commonly found in patients with locally advanced and lymph node positive disease, and it was associated with overall survival. However, recurrence-free survival was not associated with CA 125. Further studies are required to define the exact role of CA 125 in bladder cancer.	bladder
Early evaluation of hematuria in a patient receiving anticoagulant therapy and detection of malignancy.	A 63-year-old Caucasian man had a painless episode of dark-colored urine while taking warfarin 62.5 mg/week for lone atrial fibrillation in the presence of documented stable anticoagulation. Urinalysis revealed microscopic hematuria. Three weeks later, he had an episode of gross, painless hematuria. Thorough evaluation of the upper and lower urinary tract with renal ultrasound, intravenous pyelography, and cystoscopy revealed poorly differentiated, early-stage, transitional cell carcinoma of the bladder. The patient was not aware of any exposure to carcinogens known to predispose to bladder cancer, nor was he a tobacco user. Early identification of the malignancy allowed for aggressive surgical intervention. Although this patient was considered low risk for the development of bladder cancer and was taking anticoagulants, the presence of hematuria was indicative of underlying pathology. Timely and thorough evaluation of hematuria in patients taking anticoagulants is necessary to identify and treat clinically important pathology.	bladder
Polymyositis associated with urinary bladder cancer: an autopsy case.	A 56-year-old man suffered from muscle weakness with elevated serum creatine kinase. Under diagnosis of polymyositis, the patient was treated with corticosteroid, methotrexate and cyclosporin A. Eleven months after the first signs of muscle weakness, the patient suffered an abrupt onset of anuria and underwent hemodialysis. The patient died of respiratory insufficiency 14 months after the first signs of muscle weakness. Autopsy findings revealed associated urinary bladder cancer with histological indications of adenosquamous cell carcinoma, liver metastasis and cancerous lymphangitis of the lung.	bladder
Management of endosalpingiosis of urinary bladder.	We report on a 48-year-old woman who presented with abnormal uterine bleeding secondary to uterine fibroids and who was found to have incidental endosalpingiosis of the urinary bladder. Follow-up is necessary for bladder endosalpingiosis because of its tendency to recur. Follow-up should include cystoscopy and renal, and possibly pelvic, ultrasonography.	bladder
[Study of the angiogenesis as prognostic factor of pT1G3 bladder tumours].	"INTRODUCTION AND OBJECTIVES: Angiogenic activity has been considered like prognostic factor in several solid tumors. This activity can be analysed by two ways: immunohistochemical determination of molecules that activate/inhibit angiogenesis or quantitive measure of microvascular density (MD). Our objective is to determine the prognostic value of Vascular Endothelial Growth Factor (VEGF) and Microvascular Density (MD) in pT1G3 bladder tumours. MATERIAL AND METHODS: We have studied retrospectively 83 patients with pT1G3 tumors treated by TUR + endovesical instillations with a follow up of 3 years at least. We analysed VEGF expression monoclonal antibody No. 360P. To determine MD we have marked vessels with FVIII antibody and detected ""hot spots"" areas. The number of microvessels is quantited by a digital image analyser excluding those that have more than 50 micras of diameter. We established the correlation of these findings with recurrence, progression and survival by using Chi-square test and Kaplan-Meier curves (log-rank). RESULTS: Average follow up was 58 +/- 28 months. We have established like cut-off 50% of tumor cells (VEGF) and 30 microvessels/fields (MD). Chi-square test did not show correlation with survival neither recurrence but it was positive for progression p(VEGF) 0.048 and p(DM) 0.021. Kaplan Meier curves determined significative differences only for free of progression time respect to MD (p 0.038). CONCLUSIONS: We did not find statistically significant value for recurrence nor survival. Just MD reached prognostic value for progression. More studies and multivariant analysis are required to determine the clinical utility of MD, specially in order to make more aggressive therapeutic options in this kind of patients."	bladder
[Medical treatment of cancer in the elderly].	Paralleling increasing life expectancy, the number of cases of cancer in our population is also on the increase. The question as to whether chemotherapy for the treatment of a tumor in the elderly is appropriate or not, and if so what doses are required, depends in particular on the potentially increased toxicity of the drug in the old patient. The consequence is that alternative substances may have to be sought. When planning treatment, however, additional factors have to be taken into account, such as the possibility of differences in the physiology of the tumor in the elderly, the general state of health of the patient, the presence of concomitant diseases, possible interactions with other medications, and the patient's social environment.	bladder
'Will you be doing my operation doctor?' Patient attitudes to informed consent.	BACKGROUND: As part of the consent process, it is part of a doctor's duty of care to reveal any material risk. Depending upon the level of supervision, whether the operating surgeon is a trainee may be such a risk, but in our experience this is not routinely discussed with patients pre-operatively. We set out to discover patients' attitudes to being operated on by trainee urological surgeons. PATIENTS AND METHODS: A total of 101 completed questionnaires were received from patients (90 male, 11 female, mean age 72 years) undergoing transurethral resection of the prostate (TURP), transurethral resection of a bladder tumour (TURBT) or cystodiathermy on various aspects of their attitudes to being operated on by junior doctors as part of training. RESULTS: The response rate was 77%. Of the respondents, 94 patients (91%) thought that junior doctors should perform surgery as part of their training. Only 11 of 73 (15%) said they would be happy for a junior doctor, competent to perform the procedure, to operate unsupervised. Of 98 patients, 80 (82%) thought they should be told if the operation was going to be performed by a junior doctor, and 85 (87%) that they should be told their name and designation. CONCLUSIONS: For consent to be 'informed', the experience and identity of the surgeon should be made known to patients. Most patients are happy to be operated on by a junior doctor under consultant supervision, but would want to be told and know their name and status.	bladder
NMP22 BladderChek Test: point-of-care technology with life- and money-saving potential.	A new, relatively obscure tumor marker assay, the NMP22 BladderChek Test (Matritech, Inc.), represents a paradigm shift in the diagnosis and management of urinary bladder cancer (transitional cell carcinoma). Specifically, BladderChek should be employed every time a cystoscopy is performed, with corresponding changes in the diagnostic protocol and the guidelines of the American Urological Association for the diagnosis and management of bladder cancer. Currently, cystoscopy is the reference standard and NMP22 BladderChek Test in combination with cystoscopy improves the performance of cystoscopy. At every stage of disease, BladderChek provides a higher sensitivity for the detection of bladder cancer than cytology, which now represents the adjunctive standard of care. Moreover, BladderChek is four-times more sensitive than cytology and is available at half the cost. Early detection of bladder cancer improves prognosis, quality of life and survival. BladderChek may be analogous to the prostate-specific antigen test and eventually expand beyond the urologic setting into the primary care setting for the testing of high-risk patients characterized by smoking history, occupational exposures or age.	bladder
Novel recurrent structural chromosomal aberrations in primary bladder cancer.	BACKGROUND: Bladder cancer is a heterogeneous genetic disease and, to date, no specific cytogenetic abnormality has been established. The detection of recurrent genetic changes with common breakpoints is of special interest, facilitating the identification of genes implicated in carcinogenesis. The aim of this study was to investigate recurrent structural chromosomal aberrations with common breakpoints and to correlate them with the histological stage of tumors. MATERIALS AND METHODS: Fifteen patients with transitional cell carcinoma of the bladder were cytogenetically studied by direct culture of primary tumor cells and G-banding technique. RESULTS: Most of the cases studied exhibited very complex karyotypes. Recurrent structural aberrations were observed involving, according to frequency, chromosomal regions 11p15, 3p12, 14q32, 19q13 and 6q23. Isochromosomes i(8q), i(17q) and i(6p) were also observed. CONCLUSION: Conventional cytogenetics continues to be valuable in cancer study, detecting common chromosomal breakpoints. Of interest was the detection of novel recurrent structural chromosomal aberrations including involvement of 11p15, 14q32 and 19q13, while a correlation of recurrent abnormalities observed with tumor stage was also evaluated.	bladder
Carboxyamido-triazole (CAI), a signal transduction inhibitor induces growth inhibition and apoptosis in bladder cancer cells by modulation of Bcl-2.	Pro- and anti-apoptotic factors and intracellular signaling pathways are targets for therapeutic development of anticancer agents. Carboxyamido-triazole (CAI) is an inhibitor of transmembrane calcium influx and intracellular calcium-requiring signal transduction pathways. The present study investigates the effects of CAI on human transitional cancer cell (TCC) viability and apoptosis, and evaluates whether apoptotic resistance may be overcome pharmacologically. Both well-differentiated (RT4, RT112/grade 1) and poorly-differentiated (T24/grade 3; SUP/grade 4) human TCC lines were shown to express Fas. Upon exposure to agonistic monoclonal Fas antibody, only well-differentiated TCC lines underwent apoptotic cell death. CAI exposure reduced cell viability and caused an at least additive anti-apoptotic effect in combination with the Fas antibody in the Fas-insensitive TCC lines. Under the same conditions under which CAI treatment augmented Fas-mediated apoptosis, it was shown to reduce intracellular bcl-2 quantity. This response to CAI indicates that apoptotic cell death is enhanced by the reduction of bcl-2 protein expression. We suggest that the antitumor effect of CAI is at least partially based on restoring a pathway of apoptosis. It may cause transformation of cell homeostasis that leads to the alteration of apoptotic mechanisms, thus allowing highly malignant tumor cells to re-enter the physiological course of cell elimination.	bladder
Inhibition of human bladder tumour cell growth by fibroblast growth factor receptor 2b is independent of its kinase activity. Involvement of the carboxy-terminal region of the receptor.	The b isoform of fibroblast growth factor receptor 2, FGFR2b/FGFR2-IIIb/Ksam-IIC1/KGFR, a tyrosine kinase receptor, is expressed in a wide variety of epithelia and is downregulated in several human carcinomas including prostate, salivary and urothelial cell carcinomas. FGFR2b has been shown to inhibit growth in tumour cell lines derived from these carcinomas. Here, we investigated the molecular mechanisms underlying the inhibition of human urothelial carcinoma cell growth following FGFR2b expression. Using a nylon DNA array, we analysed the gene expression profile of the T24 bladder tumour cell line, transfected or not with a construct encoding FGFR2b. The expression of FGFR2b in T24 cells decreased insulin-like growth factor (IGF)-II mRNA levels. This decrease was correlated with a decrease in IGF-II secretion and may have been responsible for the observed inhibition of cell growth because the addition of exogenous IGF-II restored growth rates to normal levels. Using SU5402, an inhibitor of FGFR tyrosine kinase activity, and a kinase dead mutant of the receptor, FGFR2b Y659F/Y660F, we also demonstrated that the growth inhibition and decrease in IGF-II secretion induced by FGFR2b did not require tyrosine kinase activity. Finally, we demonstrated the involvement of the distal carboxy-terminal domain of the receptor in decreasing IGF-II expression and inhibiting T24 cell growth, as Ksam-IIC3, a variant of FGFR2b carrying a short carboxy-terminus, neither downregulated IGF-II nor inhibited cell proliferation. Our data suggest that FGFR2b inhibits the growth of bladder carcinoma cells by reducing IGF-II levels via its carboxy-terminal domain, independent of its tyrosine kinase activity.	bladder
Twenty-three years of disease-free survival following cutaneous metastasis from a primary bladder transitional cell carcinoma.	We present a case of cutaneous metastases from a primary bladder transitional cell carcinoma (TCC), with a prolonged survival of 23 years. Cutaneous metastases from primary bladder TCC are uncommon and, like all metastases, have a poor prognosis. The common modality of treatment of cutaneous metastases from a primary bladder cancer is wide local excision of the metastases followed by combination chemotherapy. Here, we present a case of a solitary cutaneous metastasis from a primary bladder TCC, which was treated with wide local excision and single agent chemotherapy. Twenty-three years on, the patient remains disease and recurrence free.	bladder
Mucinous adenocarcinoma of the renal pelvis associated with transitional cell carcinoma in the renal pelvis and the bladder.	We report a case of mucinous adenocarcinoma of the renal pelvis associated with bladder carcinoma in situ (CIS). Transitional cell carcinoma (TCC) of the renal pelvis and CIS were also observed adjacent to the adenocarcinoma. Immunohistochemical assessment of the pelvic adenocarcinoma revealed positive expressions for mucin, epithelial membrane antigen, cytokeratin 7, cytokeratin 19 and carcinoembryonal antigen, but not vimentin or chromogranin. Based on the histopathological examinations, the adenocarcinoma of the renal pelvis in the present case may have a similar biological nature to conventional TCC and probably originated by development of pre-existing TCC of the renal pelvis.	bladder
Carcinomas with micropapillary morphology: clinical significance and current concepts.	Invasive micropapillary carcinoma has been recently recognized as a rare but distinctive variant of carcinoma in various anatomic sites, including breast, urinary bladder, lung, and major salivary glands. Morphologically, it is characterized by small tight clusters of neoplastic cells floating in clear spaces resembling lymphatic channels. Most often this growth pattern is mixed with a variable component of conventional carcinoma or other variants. In addition to a unique morphology, tumors with invasive micropapillary growth share a high propensity for lymphovascular invasion and lymph node metastases. Patients have typically high-stage disease at presentation and a poor clinical outcome compared with that of patients with conventional carcinoma arising in the same organ site. In this article the author reviews the available literature on tumors displaying a micropapillary component.	bladder
[The significance of the expression of cyclooxygenase-2 in bladder transitional cell carcinoma tissues].	OBJECTIVE: To investigate the expression of cyclooxygenase-2 (COX-2) in bladder transitional cell carcinoma tissues, and understand its clinical significance. METHODS: Reversal transcription polymerase chain reaction (RT-PCR) was used to assess the expression of COX-2 mRNA in 52 cases of bladder transitional cell carcinoma tissues and 17 cases of normal bladder tissues far from neoplasm; Western blot was used to assess the expression of COX-2 protein in 49 cases of bladder cancerous tissues and 17 cases of normal tissues. RESULTS: Positive expression of COX-2 mRNA was detected in 83% (43/52) of bladder cancer tissues and in 29% (5/17) of normal tissues by RT-PCR and there was significant difference in expression of COX-2 mRNA between cancer tissues and normal tissues. Western blot analysis showed that expression of COX-2 protein was correlation with the stage and grade of cancer. CONCLUSION: COX-2 is overexpressed in bladder transitional cell carcinoma. COX-2 maybe play a certain role in carcinogenesis and progression of bladder cancer and turn into a useful target of chemoprevention of bladder cancer.	bladder
Cancers of the bladder.	Bladder cancer is the fifth most common malignancy in Europe and the fourth most common malignancy in the United States. It affects one in 4000 people and accounts for 5% of all diagnosed cancers. The peak incidence is in the fifth and seventh decade. There is a strong association between smoking and bladder cancer. Smokers have a fourfold higher incidence of developing bladder cancer than the general population. The disease has a spectrum of clinical severity varying from superficial bladder cancer to muscle invasive or metastatic disease which carries a poor prognosis. Currently the superficial form of the disease is managed by endoscopic resection of the tumour, often followed by the instillation into the bladder of cytotoxic agents. Due to the tendency of bladder cancer to recur repeated cystoscopies and resections are often required. Because of this, one of the main thrusts of research is to find a way of preventing the progression from superficial disease to muscle invasive and metastatic bladder cancer.	bladder
Alteration of the MDM2-p73-P14ARF pathway related to tumour progression during urinary bladder carcinogenesis.	Transitional cell carcinomas (TCC) of the urinary bladder develop by a multistep process characterized by various stages of transformation differing in their grade of malignancy and biological behaviour. Since the prospective clinical outcome cannot be reliably predicted on histopathological grounds, we analysed the mRNA expression of the MDM2-p73-P14ARF tumour surveillance pathway in an attempt to detect alterations of gene activity, allowing a better understanding of the mechanisms responsible for conversion of low to high malignant TCC. Expression of the mRNA was determined in 71 TCC of various grades and stages using the real-time quantitative reverse transcription-polymerase chain reaction. The MDM2-p73-P14ARF pathway was dominated by the MDM2 gene, the mRNA expression of which proved to be significantly (5-fold) lower in advanced high-grade, high-stage than in superficial low-grade, low-stage TCC. Conversely, the expression of p73 mRNA increased with increasing tumour grades and stages, while the activity of the P14ARF gene was not substantially altered during early and late phases of urothelial carcinogenesis. Analysing the expression of spliced variants of MDM2 mRNA, we found a heterogeneous pattern including a novel splicing transcript coding for an abnormal protein. Promoter hypermethylation of P14ARF occurred in 10% of the TCC with an under-expression of mRNA. An analysis of the effects of lifestyle and occupational bladder cancer risk factors revealed that TCC of smokers showed a 2-fold elevated expression of MDM2 mRNA and an approximately 2-fold lower expression of P14ARF mRNA, whereas the activity of the p73 gene was unchanged. Heavy coffee consumption was associated with a 2-fold decreased expression level of P14ARF mRNA. Exposure to certain occupational hazards (plastic products, paints and lacquer, polycyclic hydrocarbons, chemical solvents) was observed to modulate the activity of the genes analysed. Our findings suggest that an alteration in the MDM2-p73-P14ARF pathway is involved in the progression of bladder cancer to a more malignant and aggressive form.	bladder
Expression and regulation of MIM (Missing In Metastasis), a novel putative metastasis suppressor gene, and MIM-B, in bladder cancer cell lines.	It has been proposed that a 356 amino acid protein encoded by the MIM (Missing In Metastasis) gene on Chromosome 8q24.1, is a bladder cancer metastasis suppressor. Recently, Machesky and colleagues [Biochem. J. 371 (2003) 463] identified MIM-B, a 759 amino acid protein, of which the C-terminal 356 amino acids are almost identical to MIM. Importantly, PCR primers and Northern Blotting probes used in the studies of MIM in bladder cancer did not distinguish between sequences specific for MIM or MIM-B, thus the importance of either protein to bladder cancer remains unclear. We have used primer sequences specific for either MIM or MIM-B to explore the possible functional significance of MIM and MIM-B to bladder cancer cell behaviour. We have compared MIM and MIM-B mRNA levels in a non-tumourigenic, non-invasive, transformed uro-epithelial cell line versus 15 bladder cancer cell lines of differing in vitro invasive abilities, as well as in five cell lines clonally isolated from the BL17/2 bladder tumour cell line, whose in vitro and in vivo invasive abilities have been determined. MIM and MIM-B mRNA levels varied widely between cell lines. Down-regulation of MIM and MIM-B occurred in 6/15 (40%) lines but lines showing down-regulation differed between MIM and MIM-B. Reduced levels of MIM and MIM-B in BL17/2 were further reduced in 2/5 (40%) sublines (MIM and MIM-B). Importantly, there was no association between MIM or MIM-B expression and invasive behaviour in vivo or in vitro. Treatment of representative cell lines with 5-aza-2-deoxycytidine failed to induce MIM or MIM-B expression. Furthermore, there was no association between MIM or MIM-B mRNA levels and p53 functional status. Our data indicate that down-regulation of MIM and/or MIM-B expression can occur in bladder cancer cell lines but is not associated with increased invasive behaviour. Our data also suggest that in those cell lines with reduced levels of MIM and MIM-B mRNA, down-regulation is unlikely to be due to promoter hypermethylation or loss of p53 function.	bladder